Arsenic is a toxic heavy metal vastly dispersed all over the earth crust. It manifests several major adverse health issues to millions of arsenic exposed populations. Arsenic is associated with different types of cancer, cardiovascular disorders, diabetes, hypertension and many other diseases. On the contrary, arsenic (arsenic trioxide, As2O3) is used as a chemotherapeutic agent in the treatment of acute promyelocytic leukemia. Balance between arsenic induced cellular proliferations and apoptosis finally decide the outcome of its transformation rate. Arsenic propagates signals via cellular and nuclear pathways depending upon the chemical nature, and metabolic-fates of the arsenical compounds. Arsenic toxicity is propagated via ROS induced stress to DNA-repair mechanism and mitochondrial stability in the cell. ROS induced alteration in p53 regulation and some mitogen/ oncogenic functions determine the transformation outcome influencing cyclin-cdk complexes. Growth factor regulator proteins such as c-Jun, c-fos and c-myc are influenced by chronic arsenic exposure. https://www.selleckchem.com/products/Vorinostat-saha.html In this review we have delineated arsenic induced ROS regulations of epidermal growth factor receptor (EGFR), NF-ĸβ, MAP kinase, matrix-metalloproteinases (MMPs). The role of these signaling molecules has been discussed in relation to cellular apoptosis, cellular proliferation and neoplastic transformation. The arsenic stimulated pathways which help in proliferation and neoplastic transformation ultimately resulted in cancer manifestation whereas apoptotic pathways inhibited carcinogenesis. Therapeutic strategies against arsenic should be designed taking into account all these factors.Lanmuchang mercury-thallium mine, a typical polymetallic mine is located in southwestern Guizhou, China, is the most serious and typical area resulted from multi-metal contamination (Tl, Hg, As, and Sb). After the mercury-thallium mining, a large area of surrounding rocks such as argillaceous sandstone with high contents of Tl, Hg, As, and Sb is exposed to air. Weathering caused the argillaceous sandstone to form different weathering layers, including the grey-black external layer, the brown-yellow middle layer and the gray-white inner layer, and the external layer was enriched with higher heavy metals. However, the reason of heavy metal migration and transformation in argillaceous sandstone caused by weathering is unclear. The objective of this paper was to investigate the migration, transformation and release characteristics of Tl, Hg, As, and Sb in argillaceous sandstone during the weathering. The results indicated that weathering not only promoted an acidic oxidation environment in argillaceous sandstone,ng minerals, showing enrichment phenomena, partially released into the environment, causing environmental pollution.Contamination of agricultural land and water by heavy metals due to rapid industrialization and urbanization including various natural processes have become one of the major constraints to crop growth and productivity. Several studies have reported that to counteract heavy metal stress, plants should be able to maneuver various physiological, biochemical and molecular processes to improve their growth and development under heavy metal stress. With the advent of modern biotechnological tools and techniques it is now possible to tailor legume and other plants overexpressing stress-induced genes, transcription factors, proteins, and metabolites that are directly involved in heavy metal stress tolerance. This review provides an in-depth overview of various biotechnological approaches and/or strategies that can be used for enhancing detoxification of the heavy metals by stimulating phytoremediation processes. Synthetic biology tools involved in the engineering of legume and other crop plants against heavy metal stress tolerance are also discussed herewith some pioneering examples where synthetic biology tools that have been used to modify plants for specific traits. Also, CRISPR based genetic engineering of plants, including their role in modulating the expression of several genes/ transcription factors in the improvement of abiotic stress tolerance and phytoremediation ability using knockdown and knockout strategies has also been critically discussed.Microcystin-leucine arginine (MC-LR) is a kind of toxin produced by cyanobacterial, resulting in decrease of testosterone levels in serum and leading to impaired spermatogenesis. Gonadotropin-releasing hormone (GnRH) neurons play crucial roles in the regulation of testosterone release. Meanwhile, it has been demonstrated that MC-LR is capable of entering the GnRH neurons and inducing apoptosis. Nevertheless, the molecular mechanism of MC-LR induced apoptosis of GnRH neurons remains elusive. In present study, we found that MC-LR inhibited the cell viability of GT1-7 cells. In addition, we discovered apoptosis of GnRH neurons and GT1-7 cells treated with MC-LR. And increased intracellular ROS production and the release of intracellular Ca2+ were all observed following exposure to MC-LR. Furthermore, we also found the endoplasmic reticulum stress (ERs) and autophagy were activated by MC-LR. Additionally, pretreatment of the ERs inhibitor (4-Phenyl butyric acid) reduced the apoptotic rate of GT1-7 cells comparing with MC-LR exposure alone. Comparing with MC-LR treatment alone, apoptotic cell death was increased by pretreatment of GT1-7 cells with an autophagy inhibitor (3-methyladenine). Together, our data implicated that the treatment of MC-LR induced the apoptosis of GnRH neurons by activating the ERs resulting in a decrease of serum testosterone level in mice. Autophagy is a protective cellular process which was activated by ER stress and thus protected cells from apoptosis upon MC-LR exposure.Residues of the psychoactive drug diazepam (DZP) may pose potential risks to fish in aquatic environments, especially by disrupting their behavioral traits. In this study, female and male zebrafish were subjected to chronic exposure (21 days) to sublethal doses (120 and 12 ?g/L) of DZP, aimed to compare the characteristics of their behavioral responses to DZP exposure, and to investigate the possible links between those behavioral responses and variations in their brain γ-aminobutyric acid (GABA) and acetylcholinesterase (AChE) levels. Chronic exposure to DZP significantly decreased the swimming velocity and locomotor activity of both genders, indicating a typical sedative effect. Compared with males, whose locomotor activity was only significantly decreased by exposure to DZP for 21 days, females became hypoactive on day 14 (i.e., more sensitive), and they developed tolerance to the hypoactive effect induced by 120 μg/L DZP by day 21. Exposure to DZP significantly disturbed the behavioral traits related to social interactions in females but not in males.